Poison Ivy, Poison Oak and Other Plants that Contain Urushiol
Poison ivy (Toxicodendron radicans), poison oak (Toxicodendron diversilobum), poison sumac, and various other similar plants cause allergic contact dermatitis in people. These plants are variously found throughout the United States. A subspecies of poison ivy (T. radicans; ssp. Divaricatum) is native to southern Baja Calif. and Sonora, Mexico. Reports show that there are at least four native species of Toxicodendron in North America, including seven subspecies of poison ivy, and three species in Malaysia and China, including two subspecies of poison ivy, one in China and one in Japan.
Poison oak is a widespread deciduous shrub throughout the mountains and valleys of California, generally at elevations below 5,000 feet. In some locations it grows as a climbing vine with aerial (adventitious) roots that adhere to the trunks of oaks and sycamores. Poison oak also forms dense thickets in chaparral and coastal sage scrub, particularly in central and northern California. Poison oak regenerates readily after disturbances such as fire and the clearing of land. Rocky Mountain poison oak (Toxicodendron rydbergii) occurs in canyons throughout the Western United States and Canada. Because the two species of Western poison oak often exhibit a viney growth form, they are considered to be subspecies of Eastern poison ivy.
The pinnately trifoliate leaves typically have three or five leaflets, the terminal leaf being on a slender rachis (e.g., a stalk or petiolule). Eastern poison ivy often has a longer rachis and the leaflet margins tend to be less lobed and serrated (i.e., less “oak-like”). In the similar-appearing squaw bush (Rhus trilobata) the terminal leaflet is sessile (without a stalk). Like many members of the Sumac Family (Anacardiaceae) new foliage and autumn leaves often turn brilliant shades of pink and red due to anthocyanin pigments. In the Eastern United States poison ivy is often mistaken for another common native called Virginia creeper (Parthenocissus quinquefolia), which has a similar growth habit and attractive autumn foliage, but with five leaflets rather than three. Virginia creeper belongs to the grape family (Vitaceae) along with the common wild grape (Vitis girdiana).
In poison ivy, during the late spring loose clusters (panicles) of small greenish-white flowers are produced in the leaf axils. Functional male and female flowers are typically produced on separate plants (dioecious), or occasionally, unisexual and bisexual flowers may occur on the same plant (polygamous). Male flowers contain five stamens and a rudimentary pistil surrounded by five cream-colored petals and five sepals. Female flowers have a fertile pistil (gynoecium) and reduced, sterile stamens. During summer and fall, female plants produce small clusters of ivory-white fruits, each with a papery outer exocarp, a soft waxy mesocarp and a hard stony endocarp surrounding the seed. The fruits of related shrubs such as squaw bush, lemonadeberry (Rhus integrifolia) and sugar bush (Rhus ovata) are reddish with a sticky-pubescent exocarp. The old adage about poison oak and poison ivy is quite accurate: “Leaves of three, let it be; berries white, poisonous sight.”
Freshly cut stems exude a sticky, terpene oleoresin that oxidizes and polymerizes into a shiny black lacquer resembling pruning sealer. The resinous sap is produced in resin canals of the stems, roots, leaves and flowers. Cross sections of poison oak stems show distinct concentric annual rings (ring-porous wood). Numerous resin canals appear as tiny black dots and are confined to the phloem layer just inside the bark. Dark resin canals (appearing as black striations) also occur in the waxy mesocarp of the fruits just beneath the papery skin. Abundant resin canals is one of the reasons poison oak and poison ivy are placed in the genus Toxicodendron rather than the older genus Rhus. Toxicodendron is also the updated generic name for poison sumac (T. vernix) and the Japanese lacquer tree (T. vernicifluum), the commercial source of natural lacquer. The resin canals also contain urushiol, the insidious allergen that gives poison oak its bad reputation. The name is derived from “urushi”, Japanese name for lacquer made from the sap of the Japanese lacquer tree (“kiurushi” or “urushi ki”).
In addition to poison oak, poison ivy and poison sumac, a number of other species in the Sumac Family contain urushiol mixtures. In Japan, dermatitis reactions have been reported from contact with lacquered objects (from Japanese lacquer tree) such as bar tops, rifle stocks and toilet seats. Dermatitis has also been reported in people handling mangoes (Mangifera indica), shells of cashew nuts (Anacardium occidentale), the Rengas tree (Gluta renghas), Burmese lacquer tree (Melanorrhoea usitata) and two attractive Caribbean shrubs, Metopium toxiferum and Comocladia dodonaea. The name Rengas actually refers to several genera of large Malaysian trees with resinous sap that blackens when exposed to the air. Urushiols also occur in the seeds of Ginkgo biloba (Ginkgoaceae) and in several genera of the Proteaceae.
Urushiol Oil, Structure and Transport
Urushiol is the broad term given to the substance in the sap of poison ivy (Toxicodendron radicans), poison oak (Toxicodendron diversilobum), poison sumac, and other plants that causes allergic contact dermatitis in people. Urushiol is a clear, sticky oil, causes an allergic reaction, and is potent even on dead or dried plants, which causes urushiol to be hazardous even during the winter months. Some reports estimate that between approximately 50% and 70% of the U.S. population is allergic to urushiol. In fact, there is some clinical evidence shows that no one is completely immune to the urushiol but that the sensitivity is a matter of degree: some people are sensitive to small amounts while others react only to large amounts. Poison oak and poison ivy account for an estimated ten percent of lost work time in the U.S. Forest Service. In fact, hundreds of fire fighters who battle summer and fall blazes in California's coastal ranges are so severely affected that they are unable to work. People who breathe in the smoke and soot may develop serious inflammation of respiratory mucous membranes. Because of the serious economic impact due to lost employment time, poison oak “injuries” are covered by Workers' Compensation Insurance in California. It is reported that the monetary cost of this affliction is approximately one percent of the state's workers' compensation budget.
Reports indicate that urushiol is actually a mixture of phenolic compounds that are known as catechols, which are potent benzene ring compounds having a long side-chain of 15 or 17 carbon atoms. The side chain may be saturated or unsaturated with one, two, or three double bonds. It is reported that the immune reaction and specificity of the catechol molecule is determined by the long side-chain. Poison oak urushiol contains mostly catechols with 17 carbon side-chains (heptadecylcatechols), while poison ivy and poison sumac contain mostly 15 carbon side-chains (pentadecylcatechols). These compounds are illustrated below. Formula I depicts the chemical structure of urushiol in which there are five possibilities for the variable R:
R═(CH2KH3)  IR═HC═CH(CH2)5CH3  IIR═HC═CHCH2CH═CH(CH2)2CH3  IIIR═HC═CHCH2CH═CHCH═CHCH3  IVR═HC═CHCH2CH═CHCH2CH═CH2  V
Formula II depicts the chemical structure of the pentadecylcatechols in which there are four possibilities for the variable R:
R═C15H31, C15H29, C15H27 and C15H25 
Formula III depicts the chemical structure of the heptadecylcatechols in which there are four possibilities for the variable R:
R′═C17H35, C17H33, C17H31 and C17H29 
The above figures illustrate the chemical structure of urushiols found in resin canals of poison oak and poison ivy. Poison ivy mostly contains a mixture of four saturated pentadecylcatechols (with 15-carbon side chain), while poison oak contains a mixture of four heptadecylcatechols (with 17-carbon side chain).
As indicated above, the side chain may be saturated or unsaturated with one, two, or three double bonds. According to some studies, the immune reaction and specificity of the catechol molecule is a function of the long side-chain. As might be expected, the urushiol can vary based on the plant in which it is found. For example, the urushiol from poison oak contains mostly catechols with 17-carbon side-chains (heptadecylcatechols). In contrast, the urushiol from poison ivy and poison sumac contain mostly 15 carbon side-chains (pentadecylcatechols).
It has been reported that urushiol is found in only the resin canals of the plant and that it will be found on the plant's outer surfaces only if the leaves and stems are bruised or attacked by chewing/sucking insects such that it can reach the outer surface. Although nonvolatile, it may be carried in ash and dust particles and as minute droplets in smoke from burning foliage. Many surprised people and firefighters have learned to their detriment that although urushiol is nonvolatile, it is carried in ash and dust particles and as minute droplets in smoke from burning foliage. Thus, carefully clearing poison ivy and other urushiol-containing plants with diligence to avoid contact, but then burning them creates a urushiol-containing smoke that disperses the urushiol over a great area, including the eyes and lungs. Firefighters regularly encounter this hazard when fighting forest fires.
The Body's Reaction to Urushiol
Urushiol causes an irritating skin reaction on many people. The body's immune system treats urushiol as foreign and attacks the complex of urushiol-derivatives with skin proteins. In the absence of the immune attack, urushiol would be harmless. The reaction, an itchy rash with clear blisters, is variable in severity among people, and can vary from year to year on the same individual. Once the skin has been exposed to urushiol it is only a matter of hours, usually 24 to 72, before rash breaks out. Any area that comes into contact with the oil will react, except the mucous membranes, such as lips, mouth, and inside of the nose. The rash, Rhus dermatitis, starts off as red, swollen patches, with a few small fluid-filled blisters. As the reaction intensifies, the blisters become larger, and then break down and weep. The whole area becomes covered with an oozing, scaling crust. Contrary to popular belief, the rash itself does not “spread” like an infection. It is the unknowing transfer of the oil to other parts of the body by touching that gives the spreading affect. Once the oil is completely removed from skin and clothing, no further rash will result. Some rashes will appear sooner than others depending on the sensitivity of the skin area and the amount of urushiol contacted.
The poison ivy reaction can be reduced by changing clothing immediately after contact and washing the exposed skin with soap and water. It is reported that if a person can wash all the oil off exposed skin within 5 minutes of contact, no reaction will occur. Even water from a running stream can be an effective cleanser. Some people are so sensitive to urushiol that it only takes a molecular trace of urushiol (two micrograms or less than one millionth of an ounce) on the skin to initiate an allergic reaction. Even the amount on a surface the size of pinhead is sufficient to cause rashes in 500 sensitive people. Approximately 80-90 percent of adult Americans will get a rash if they are exposed to 50 micrograms of purified urushiol, which is a minute amount when considering that one grain of table salt weighs about 60 micrograms. An urushiol residue on the skin is difficult to wash off and may be spread by scratching. Contrary to popular belief, it is not spread through blister fluids. It is a relatively stable compound and can retain its potency for years in the absence of oxidation—herbarium specimens 100 years old have been known to cause dermatitis. Urushiol is readily transferred from contaminated clothing, objects and fur of animals. Moreover, it readily penetrates the epidermal layer of the skin where it binds to proteins of deeper skin cell membranes. Before the protein bond can occur the catechol (Formula IV) is oxidized to a more reactive quinone (Formula V) in which the two OH groups are replaced by double-bonded oxygens, as illustrated in the reaction schematic FIGURE below.

The above illustration shows the chemical structure of poison oak urushiol (heptadecylcatechol) and its oxidized “reactive” quinone. The reactive quinone bonds to white blood cell membranes deep in the skin.
In the conjugated state (bound to cell membranes) urushiol is virtually impossible to wash off. By itself the urushiol molecule (also called a hapten) probably would not initiate a full-blown immune response, but when attached to the cell membrane it becomes a “warning flag” that attracts patrolling T-cells.
Poison oak urushiol causes a complicated delayed allergic reaction with the body's immune system. It is technically classified as a cell-mediated immune response and the “peak misery” may not appear until days or weeks later. It is quite different from the primary irritants of nettle and euphorbias, the effects of which are immediate. The following hypothetical “two-phase” scenario for poison oak dermatitis is summarized from the scientific literature. PHASE I (Induction): Initial contact with poison oak may result in urushiol penetrating the stratified squamous epithelial cells of the skin and binding to large dendritic (branched) white blood cells in the epidermis called Langerhan's cells, as illustrated in FIG. 1, which illustrates a hypothetical mechanism for the poison oak scenario: a delayed action, cell-mediated immune response.
The Langerhan's cell (with urushiol allergen and MHC protein on its membrane) migrates to a nearby lymph node where clones of special white blood cells, called effector T-cells, are programmed to recognize urushiol. Some immunology textbooks refer to these clones of T-cells, with urushiol receptor sites on their membranes, as “helper T-cells.” There are literally millions of effector T-cells (helper T-cells) roaming throughout the blood and lymphatic system, each with special receptor molecules on their membranes for a particular allergenic chemical, such as the urushiol of poison oak. T-cells patrol the body's circulatory system looking for invading cells and viruses.
PHASE II (Elicitation): Once urushiol is absorbed into the skin during a subsequent encounter with poison oak, an effector T-cell may encounter it bound to a Langerhan's cell and attach to it by a specific recognition system. The effector T-cell then produces more clones of itself and releases special proteins called lymphokines (cytokines) which attract a legion of different white blood cells, including “cell engulfing” macrophages and cytotoxic (“killer”) T-cells. The killer T-cells are also produced in regional lymph nodes during the Elicitation phase, and according to some textbooks, they also have urushiol receptors on their membranes. The new army of white blood cells releases lytic enzymes and protein toxins (perforins) which destroy everything in the vicinity including membrane-bound urushiol and other skin cells, thus producing a blistering rash. Fluid oozes from the blood vessels and lymphatics (edema) and cell death and necrosis (breakdown) of skin tissue occurs. Milder effects range from redness (vasodilation) and itching (nerve injury) to small blisters (vesicles and bullae).
There is some natural immunity to poison oak. Sensitization depends on the chance meeting of a special effector T-cell (with correct receptor site) and the poison oak allergen—a painful biochemical rendezvous. A person may not have effector T-cells with the special receptor for urushiol—or perhaps a person that has relatively few effector T-cells with precise poison oak receptor may never encounter the urushiol allergen. The allergen may be absorbed and degraded before the T-cells find it. Immunity to poison oak with age, exposure and homeopathic remedies may involve suppressor T-cells which inhibit or block the action and reproduction of other T-cells. Circulating IgG immunoglobulin antibodies that block the T-cell receptor for urushiol may also be involved.
Since the HIV virus attacks helper T-cells, persons afflicted with the deadly disease AIDS have a serious deficiency in cellular (T-cell) immunity. AIDS patients may not have problems with poison oak dermatitis and this likely reflects their decreased cellular immunity. In fact, one treatment for AIDS patients is to try to sensitize them to another allergenic chemical (dinitrochlorobenzene) in order to stimulate T-cell production.
Treatments for Urushiol-Induced Contact Dermatitis
Scientists have tried many homeopathic remedies made from extracts of poison oak. Some products, such as poison oak tablets and droplets, were withdrawn from the market because of severe allergic reactions in hypersensitive people. One area of desensitization research involves oral pills and intramuscular injections of related or modified urushiol: A molecule similar enough to urushiol to have the same immunological effect, but different enough to avert its excruciating side effects. Other research may lead to a vaccine that blocks the specific urushiol T-cell receptor and immunizes “high risk” people against urushiol for periods of time. In fact, Allergene, a biotech company in San Mateo, Calif. has successfully produced a hybridoma (fused lymphocyte and carcinoma cell) that makes urushiol-binding monoclonal antibodies. These antibodies prevented sensitized mice from reacting with urushiol.
The complete list of topical treatments for poison oak and poison ivy includes an array of materials, including bleach, morphine, kerosene, buttermilk, and gunpowder. Lotions, creams and sprays containing anti-inflammatory corticosteroids (hydrocortisones) are generally accepted as being potential effective agents to relieve painful, itching rashes. Serious outbreaks may require medical attention and hospitalization. The ideal therapy when exposed to poison oak or ivy is to wash the contaminated areas thoroughly, unfortunately most ordinary bath soaps have little effect on removing the resinous sap. There are some reports that soaps with added moisturizers and oils together with brisk rubbing may even spread the urushiol, thereby increasing the area of allergic response. Strong laundry soaps, such as Fels Naptha, may also spread the allergen and be harsh on sensitive skin. Some sources recommend antipruritic (anti-itch) agents such as calamine lotion for mild cases.
Another remedy for the discomfort of itching poison oak and ivy lesions is a “pore minimizer” acne treatment with 2% salicylic acid (available from several manufacturers, including Neutrogena® and Johnson & Johnson). A poultice made from the resinous flowers and leaves of gum plant (Grindelia robusta) was commonly used by Indians and early settlers in California to relieve inflammation and itching. Native Americans also made concentrated poultices from boiled leaves of the common shrubs yerba santa and manzanita (Eriodictyon and Arctostaphylos spp.), and from the thick roots of mule ears (Wyethia longicaulis), a resinous, balsam-scented sunflower with large basal leaves. Other reported naturopathic remedies to relieve the inflammation and itching of poison oak rashes include salves made from the crushed leaves of Aloe vera and narrow-leaf plantain (Plantago lanceolata). Some herbal manuals list a poultice made from juicy stems of the North American jewelweeds (Impatiens capensis and I. pallida), succulent wildflowers that grow with poison ivy in the Eastern states; although its efficacy is questionable and possibly amply disproved.
A recent editorial in Mushroom The Journal (Winter 1994-95) discussed a mycological cure for poison oak rash by rubbing fungi such as Boletus and Polyporus on the affected skin. This treatment is based on the fact that freshly cut pieces of mushrooms, apples and potatoes turn dark when exposed to the air. The actual mechanism for this blackening process involves the oxidation of phenolic compounds in the tissues of these pieces by the enzyme tyrosinase. The resulting quinones rapidly polymerize into a brown residue. Placing the pieces under water prevents this “unsightly” oxidation. In fact, chefs add lemon juice, which contains the strong reducing agent ascorbic acid; this keeps the phenolics reduced. Since urushiol is a phenolic compound, tyrosinase would probably also detoxify it. The enzymes might also reduce the spreading of urushiol to other parts of the body by deactivating it at the initial site of exposure.
There is a report that an even more specific and potent oxidase for urushiol, catechol 2,3 oxidase, oxidizes the ring structure between carbon atoms # 2 and # 3 and thereby destroying the molecule. In the study, a bacterial gene was cloned and expressed to produce this recombinant enzyme, which oxidized the urushiol in vitro within seconds. The report further notes that when applied to skin the enzyme sometimes prevented a rash, but only if the urushiol was inactivated before penetrating the epidermis. The efficacy of patented creams containing oxidase enzymes depends on the oxidation of urushiol at the initial site of contact before it has penetrated the skin. Once urushiol binds to the protein of skin cell membranes, these creams would have little effect on the subsequent immune response.
There are a number of commercially available products. One product, called Tecnu Oak-n-Ivy® Cleanser, is now marketed through forestry supply catalogs. Tecnu is a crude distillate of gasoline and contains a mixture of organic solvents and wood pulp by-products which remove terpene resins and urushiol from the skin. Thorough rinsing with water is recommended. Similarly, other organic solvents, including rubbing alcohol, likely would remove the urushiol residue. However, if the allergen has already penetrated the epidermal layer and bonded to deeper skin cells it is too late. Another product that claims to remove urushiol from the skin, even after a rash has developed, is called Zanfel™. Yet another product developed for the U.S. Forest Service is called Ivy Block®. It is in the form of an aerosol spray or lotion containing activated bentonite clay used in antiperspirants. Ivy Block® is described as forming a barrier that both prevents urushiol from touching the skin and chemically binds with it so it becomes inactive. Another blocking agent, called StokoGard Outdoor Cream®, is a fatty acid ester and is available through industrial supply houses and through pharmacist who can order it from Stockhausen, Inc. of Greensboro, N.C.
A number of background sources on poison ivy include: waynesword.palomar.edu/ww0802.htm, chemweb.calpoly.edu/chel'n/bailey/377/PapersF2000/Dana/, and Dana Longinetti, Chem 377-Drugs and Poisons, Fall 2000.